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Regulating posttraumatic stress disorder symptoms with neurofeedback:


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Article in Journal of Military Veteran and Family Health · March 2020


DOI: 10.3138/jmvfh.2019-0032

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EMERGING PRACTICES AND
PROGRAMS
Regulating posttraumatic stress disorder symptoms with
neurofeedback: Regaining control of the mind
Andrew A. Nicholsona, Tomas Rosb, Rakesh Jetlyc and Ruth A. Laniusd
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

ABSTRACT
Neurofeedback is emerging as a psychophysiological treatment where self-regulation is achieved through online feed­
back of neural states. Novel personalized medicine approaches are particularly important for the treatment of posttrau­
matic stress disorder (PTSD), as symptom presentation of the disorder, as well as responses to treatment, are highly het­
erogeneous. Learning to achieve control of specific neural substrates through neurofeedback has been shown to display
therapeutic evidence in patients with a wide variety of psychiatric disorders, including PTSD. This article outlines the
neural mechanisms underlying neurofeedback and examines converging evidence for the efficacy of neurofeedback as an
adjunctive treatment for PTSD via both electroencephalography (EEG) and real-time functional magnetic resonance
imaging (fMRI) modalities. Further, implications for the treatment of PTSD via neurofeedback in the military mem­
ber and Veteran population is examined.
Key words: amygdala in PTSD, brain wave oscillations, EEG neurofeedback, emotion regulation, fMRI
neurofeedback, military, NATO, neurofeedback, personalized medicine, PTSD, Veterans

RÉSUMÉ
Introduction : La rétroaction neurologique apparaît comme un traitement psychophysiologique qui permet l’autorégu­
lation par la rétroaction en ligne des états neuronaux. Méthodologie : Les nouvelles approches de médecine person­
nalisée sont particulièrement importantes pour le traitement du syndrome de stress post-traumatique (SSPT), car la
présentation des symptômes et les réponses au traitement sont hautement hétérogènes. Résultats : Il est démontré que le
fait d’apprendre à contrôler des substrats neuronaux précis grâce à la rétroaction neurologique donne des résultats théra­
peutiques chez des patients présentant un vaste éventail de troubles psychiatriques, y compris le SSPT. Discussion : Le
présent article souligne les mécanismes neuronaux sous-jacents à la rétroaction neurologique et examine des données con­
vergentes sur l’efficacité de la rétroaction neurologique comme traitement d’appoint au SSPT, à la fois par l’électroencéph­
alographie (ÉEG) et l’imagerie par résonance magnétique fonctionnelle (IRMf ). De plus, on y étudie les conséquences
de la rétroaction neurologique pour le traitement du SSPT dans la population de militaires et de vétérans.
Mots-clés : amygdale en cas de SSPT, médecine personnalisée, militaires, oscillations des ondes cérébrales, OTAN,
régulation émotionnelle, rétroaction neurologique, rétroaction neurologique par ÉEG, rétroaction neurologique par
IRMf, SSPT, vétérans

THE NEED FOR NOVEL ADJUNCTIVE all public safety personnel rescue workers2 worldwide
TREATMENTS AND PERSONALIZED is 10%. An alarming national study in Canada found
MEDICINE IN PTSD that 44% of public safety personnel screened posi-
Posttraumatic stress disorder (PTSD) is a debilitating tive for symptom clusters consistent with one or more
psychiatric disorder that can develop in the aftermath mental health disorders.3 Similarly, 13% of returning
of psychological trauma.1 The incidence of PTSD in Canadian Armed Forces personnel are diagnosed with

a Department of Psychological Research and Research Methods, University of Vienna, Vienna, Austria
b Neurology and Imaging of Cognition Lab, University of Geneva, Geneva, Switzerland
c Canadian Forces Health Services Group, Department of National Defence, Government of Canada, Ottawa
d Department of Psychology, Western University, London, Ontario
Correspondence should be addressed to Andrew Nicholson at dr.andrewnicholson@gmail.com

© Her Majesty the Queen in Right of Canada, as represented by the Journal of Military, Veteran and Family Health 3
Minister of National Defence, 2020. 6(Suppl 1) 2020 doi:10.3138/jmvfh.2019-0032
Nicholson et al

deployment-related mental disorders, including PTSD.4 ways in which a person can present with PTSD.1,18 More­
In addition, a cross-sectional World Health Organi­ over, a dissociative subtype of PTSD has been defined
zation survey, conducted in 11 countries, found that in which individuals present with additional symptoms
PTSD was associated with 20.2% of sexual assault cases.5 of depersonalization and derealization, with associated
Currently, common treatments for PTSD consist of psy­ abnormal neural circuitry in emotion regulation and
chotherapy, pharmacotherapy, or a combination thereof. fear-responding regions.1,19–22
However, dropout rates from psychological therapies, Given the diversity of brain circuits that may be
such as trauma-focused cognitive behavioural therapy involved in PTSD, modern neurofeedback technology
and eye movement desensitization, are an important may facilitate a more personalized approach to medicine
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

consideration for the military and Veteran population,6,7 when treating patients with PTSD and could also help
where a recent systematic review reported an average to improve symptoms in those individuals previously
dropout rate of one in three patients among Veterans.7 resistant to treatment. The current review will focus on
In community-based settings, only 56% of patients with the fMRI and EEG signals that are used for neurofeed­
PTSD received a minimally adequate dose of psycho­ back, together with studies that demonstrate converg­
therapy.8 A cross-national meta-analysis study suggests ing neurobiological evidence for their use as treatments
that psychotherapy is reported to be successful in only in patients with PTSD.
about 60% of cases.9 Pharmacological treatment can also
be effective in PTSD, however, research suggests a sub­ INTRODUCTION TO NEUROFEEDBACK
stantial portion of patients (41%) fail to respond to this Neurofeedback is non-invasive approach used in the
type of intervention.10,11 Further, it has been suggested treatment of a wide range of neuropsychiatric disorders,
that PTSD treatment models must extend beyond one- including PTSD.13,14,16–18,23 Many different neurofeed­
size-fits-all conceptualizations and adopt a personalized back protocols and methods exist, where treatment flex­
medicine approach to treatment if they are to adequately ibility may be particularly advantageous in PTSD, as it
reflect the evidence base and the complexity of PTSD in is a heterogeneous disorder with a wide range of symp­
Veteran populations.12 toms.1,18,19,22 Neurofeedback involves a brain-computer
Importantly, neurofeedback with both electroen­ interface that provides real-time feedback of brain ac­
cephalography (EEG) and functional magnetic reso­ tivity that individuals learn to regulate using a “closed­
nance imaging (fMRI) represent an emerging adjunc­ loop” paradigm.13,14,24 Typically, the neural signal is fed
tive treatment that allows patients to self-regulate neural back to the person as an auditory or visual signal. The
states. The underlying benefit of this treatment practice individual receives positive feedback each time progress
is that one can directly entrain and regulate neural activ­ is made toward normalizing aberrant neural activity.14,18
ity along with associated psychological symptoms.13–15 Clinicians are able to target specific neural dynamics
In a systematic review of biofeedback for psychiatric in the brain, related to PTSD symptom presentation
disorders, 70% of the studies reported a statistically- and maintenance, which allows patients to self-regulate
significant clinical improvement in the treatment of de­ pathological states.18,25 Neurofeedback protocols can be
pression or anxiety disorders.16 Furthermore, with regard used with fMRI neuroimaging to precisely target local­
to patients with PTSD, a recent cross-national systemat­ ized brain regions and related brain networks, whereas
ic review found that all 10 neurofeedback studies, which EEG neurofeedback is used to regulate more global sig­
included military members, demonstrated positive im­ nals, indicative of large-scale brain oscillations.13,14 No­
provements on at least one PTSD symptom.17 tably, EEG neurofeedback has also recently been used to
Novel adjunctive treatments are particularly import­ target more specific subcortical regions of the brain.26–28
ant for the treatment of PTSD, as it is a highly hetero­ Neurofeedback represents a closed-loop design, mean­
geneous disorder, where symptom severity and the pre­ ing continuous sensory representations of brain activity
dominance of certain symptoms greatly differs between are provided to individuals in real-time with the aim
individuals, especially in more chronic cases over time.1,18 of controlling this activity.13,14 Neurofeedback can be
Based on diagnostic criteria from the Diagnostic and Sta­ conceptualized as a “virtual mirror for neural dynam­
tistical Manual of Mental Disorders, 5th edition (DSM-5), a ics occurring within the brain”, in which this interface
classification manual used by mental health professionals, allows for the modification of such dynamics and their
there are more than 600,000 symptom combinations or corresponding psychological state(s).13

4 Journal of Military, Veteran and Family Health


doi:10.3138/jmvfh.2019-0032 6(Suppl 1) 2020
Regulating PTSD symptoms with neurofeedback

In terms of mechanisms, the direct causal pathways Recent studies suggest covariation between alpha-
that mediate neurofeedback are yet to be elucidated ful­ wave oscillations in the brain and changes in the afore­
ly. However, several theories exist. Briefly, neurofeed­ mentioned ICNs52,53 that are particularly implicated in
back has been proposed to involve Hebbian plasticity, PTSD.45 Alpha oscillations (8–12Hz) are easily mea­
homeostatic plasticity, and structural plasticity within surable with EEG and correspond to a state of resting
the brain.13,14,18,29 Neuroplasticity is a concept that is wakefulness correlated to the DMN,54,55 where patients
widely supported by research within the field, in which with PTSD are known to display decreased DMN
neurofeedback may not only alter the strength of neural connectivity at rest in key hubs of this network.40,45,46 In
circuitry connections and activity within the synapse, conjunction, PTSD patients display abnormally reduced
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

but may also directly modulate abnormal brain oscilla­ alpha oscillations, proposed to be a global index of
tions.13,14,18 In support of structural changes occurring chronic hyperarousal.13,56–58 Taken together, alpha-wave
in response to neurofeedback,30,31 a recent fMRI study oscillations are frequently a target for EEG neurofeed­
reported post-training microstructural changes with re­ back due to their associations with symptoms of hyper-
gard to white matter pathways and grey matter volume arousal in patients with PTSD, along with their ability
among areas involved in the sustained attention neuro­ to modulate autonomic activity related to the stress re­
feedback task.29 Finally, in support of homeostatic plas­ sponse13 and ICN dynamics.32
ticity, EEG neurofeedback has been shown to result in Additionally, studies have repeatedly found that
a homeostatic rebound of brain wave oscillations, which PTSD is associated with less activation in the medial
has been associated with the normalization of abnormal prefrontal cortex (mPFC), which contributes to a loss of
brain circuitry in patients with PTSD and acute symp­ top-down regulation on emotion generation areas such
tom alleviation.32 In terms of implementing neurofeed­ as the amygdala, corresponding to PTSD symptoms of
back treatment interventions specifically in patients with hyperarousal vivid-reexperiencing, and emotion under-
PTSD, several neurophysiological measures have been modulation.19,20,22,59–69 PTSD symptoms of hyperarous­
identified, which represent key targets for modulation/ al have been correlated with negative mPFC-amygdala
intervention via neurofeedback. coupling,64 where PTSD patients display reduced PFC-
amygdala connectivity as compared to controls, cor­
WHAT ARE THE NEURAL TARGETS FOR responding to reduced regulation of emotion centres
MODULATION IN PTSD? during the resting state.70
Intrinsic connectivity networks (ICNs) have been Observations of these altered patterns of neural
shown to be particularly important for proper neural functioning have driven efforts to develop novel treat­
functioning in humans. Specifically, the main ICNs ment interventions that target both large-scale neural
consist of the default mode network (DMN), central oscillations, as well as localized brain regions implicated
executive network (CEN) and salience network (SN), in PTSD symptomatology. Taken together, common
where dysfunction in these three core networks plays targets for treating PTSD via neurofeedback largely
a significant role in a broad range of psychopatholo­ consist of regulating directly abnormal alpha-based
gy.33 These ICNs have been shown to be abnormal in brain oscillations related to ICNs, as well as directly reg­
PTSD and are hypothesized to be related to specific ulating amygdala activation and associated top-down
symptom presentations within the disorder, including recruitment/control from the mPFC.18,28,32,71,72 Inter­
altered self-referential processing and social cognition estingly, empirical studies with fMRI and EEG neuro­
(DMN),34,35 cognitive dysfunction (CEN),36–38 as well as feedback signals evidence overlapping neurobiological
dysregulated arousal/hypervigilance and chronic threat mechanisms, where both approaches have been shown
monitoring (SN).33,35,37,39–50 Neuroimaging studies in to lead to plastic changes in ICN and amygdala con­
PTSD suggest an over-engagement of the SN, failure nectivity. Specifically, real-time fMRI neurofeedback
to properly recruit emotion regulation and executive targeting amygdala downregulation in PTSD patients
functioning areas within the CEN, and a breakdown of may lead to increased connectivity of the amygdala with
functional connectivity within the DMN.45,51 Indeed, PFC emotion regulation areas as well as a plastic chang­
neurofeedback has been proposed as a potential avenue es within ICNs (DMN, CEN, and SN).71,72 Similarly,
by which to normalize these network abnormalities in alpha-based EEG neurofeedback also leads to plastic
PTSD.45 changes within ICNs, with associated reductions in

Journal of Military, Veteran and Family Health 5


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Nicholson et al

hyperarousal and a shift in amygdala connectivity away between the amygdala and the PFC was found during
from innate defence and fear-processing areas, toward neurofeedback training. This study suggests that neuro­
PFC emotion regulation areas.28,32 These converging feedback may be a therapeutic protocol for dampening
mechanisms underlying EEG and fMRI neurofeedback amygdala hyperactivity and restoring emotion regula­
are explored in the subsequent sections. tion PFC regions in patients with PTSD. These results
parallel other rt-fMRI-nfb studies in healthy individu­
REAL-TIME fMRI NEUROFEEDBACK als, where self-regulation of the amygdala, as compared
IN PTSD to control regions, was shown to increase activation in
Real-time fMRI neurofeedback (rt-fMRI-nfb) involves emotion regulation PFC regions, as well as enhance
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

learning to increase or decrease activity in specific corti­ amygdala-PFC connectivity.74–76,89–91 Elsewhere, it has
cal or subcortical regions and has been used to modulate also been shown that using rt-fMRI-nfb to enhance the
neural correlates underlying psychopathology.14 Several connectivity between the PFC and the amygdala during
studies have examined the capacity to regulate emotion threat exposure in highly anxious individuals resulted in
processing by targeting neurofeedback of the amygdala reduced anxiety in the absence of feedback.92
using rt-fMRI-nfb in both healthy individuals73–78 and Finally, in terms of underlying mechanisms, an anal­
psychiatric populations, including borderline personal­ ysis exploring directional connectivity in a PTSD sample
ity disorder (BPD),79 major depressive disorder,80–82 and including military members suggested that amygdala
PTSD.71,72,83,84 downregulation involved both top-down and bottom-up
The amygdala is a region associated with the pro­ information flow with regard to observed PFC-amygdala
cessing and generation of emotions,85–87 where dysregu­ connectivity.71 These results support the hypothesis that
lated amygdala activation has been shown to be central emotion regulation may be underpinned by a reciprocal
to the development and maintenance of PTSD symp­ loop of information processing, in which information
toms.19,22,46,51,67,68,88 Indeed, attenuated top-down regu­ flows in a bi-directional manner between the amygdala
lation from the mPFC with concomitant amygdala hy­ and PFC during amygdala downregulating neurofeed­
peractivity is a neural signature critical to symptoms of back.14,71,92,94 Taken together, these studies suggest that
emotion undermodulation (i.e., hyperemotionality), hy­ rt-fMRI-nfb may be an effective means of decreasing
perarousal, and re-experiencing.19,20,22,46 Notably, direct amygdala hyperactivity and enhancing PFC activity/
amygdala regulation via rt-fMRI-nfb has been shown to connectivity in order to regulate emotion states. Inter­
also affect activation in PFC areas involved in emotion estingly, increased PFC activation has also been reported
regulation, as well as to enhance amygdala-PFC connec­ when examining neural activity, post-treatment, among
tivity.74–76,89 Neurofeedback regulation of the amygdala PTSD patients.11,88,95,96
may offer a way to therapeutically normalize the abnor­ In another Canadian research study, Nicholson
mal cortico-subcortical pathways maintaining PTSD. et al.72 also provided evidence that amygdala downreg­
Nicholson et al.71 presented the first demonstration ulation via rt-fMRI-nfb leads to plastic changes within
of successful amygdala downregulation using rt-fMRI­ ICNs, which, as previously mentioned, represent neural
nfb in patients with PTSD. Here, patients were able to targets highly implicated in PTSD that are known to
downregulate both right and left amygdala activation be associated with symptom presentation.34,40,45,46,97 In
during a symptom provocation paradigm in which pa­ this study, that included military members with PTSD,
tients viewed words associated with their trauma.71 Im­ amygdala downregulation was associated with increased
portantly, patients were also able to learn to regulate their recruitment of the left CEN over neurofeedback train­
amygdala activation on a subsequent transfer trial with­ ing runs, a finding supported by increased dorsolater­
out neurofeedback.71 Here, increased activation in the al PFC activation during the downregulate condition,
dorsolateral and ventrolateral PFC was observed in tri­ specifically.72 Critically, the literature suggests decreased
als where patients were instructed to downregulate their recruitment and functional connectivity within CEN
amygdala.71 Interestingly, these regions are known to emotion regulation PFC regions among PTSD pa­
be related to emotion regulation and executive func­ tients,37,38,45,98 where attenuated regulatory activation in
tioning, while their activation was negatively correlated the PFC is associated with PTSD symptoms of emotion
with PTSD symptoms during neurofeedback train­ undermodulation (i.e., hyperemotionality) and amyg­
ing.71 Furthermore, increased functional connectivity dala hyperactivation.19,20,22 This neurofeedback protocol

6 Journal of Military, Veteran and Family Health


doi:10.3138/jmvfh.2019-0032 6(Suppl 1) 2020
Regulating PTSD symptoms with neurofeedback

may represent a therapeutic strategy to restore activity changes in ICNs highly associated with PTSD symp­
in emotion regulation regions within the CEN in an tomatology.32,45 This included plastic modulation of the
attempt to counterbalance severe emotion undermod­ DMN involved in PTSD alterations in self-referential
ulation that is observed in PTSD.72 In the same study, processing and autobiographical memory, as well as al­
DMN recruitment related to self-referential processing terations within the SN involved in the detection of sa­
and autobiographical memory was stabilized during lient threat in the environment and hypervigilance.32,45
neurofeedback runs.72 Individuals with PTSD have been Notably, this was the first study to show that key brain
shown to maladaptively recruit the DMN during tasks networks underpinning PTSD can be volitionally mod­
that require cognitive control.97 Hence, stabilization of ulated by EEG neurofeedback with outcomes on im­
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

the DMN may represent a normalization of neural dy­ mediate symptomatology.32 Importantly, these results
namics within this network; that is, a decrease from the are supported by other alpha-based, controlled neuro­
response typically observed in PTSD patients.72 This nor­ feedback studies in healthy individuals, which display
malization may allow patients to increase recruitment lasting changes in cortical plasticity post neurofeed­
of the CEN involved in executive regulation, resulting back.103,104
in more control over emotion generation centres in the Relevant to EEG neurofeedback targeting hyper-
brain (e.g., amygdala). Taken together, these recent stud­ arousal symptoms in patients with PTSD, a subsequent
ies71,72 provide exciting, preliminary evidence that fMRI study from a Canadian laboratory aimed to investigate
neurofeedback involving downregulation of the amyg­ amygdala functional connectivity before versus after
dala in PTSD is associated with measurable changes in treatment with alpha-based neurofeedback.28 Here, pri­
ICNs and emotion regulation regions,71,72 effects similar or to neurofeedback treatment, PTSD patients displayed
to those observed using EEG signals for neurofeedback stronger amygdala connectivity to areas implicated in
in patients with PTSD.28,32 threat, emotion, and fear processing, as well as trauma
memory retrieval areas (brainstem periaqueductal gray
EEG NEUROFEEDBACK IN PTSD and hippocampus, respectively). Interestingly, after a
EEG neurofeedback consists of regulating electro­ 30-minute session of alpha-based EEG neurofeedback,
cortical oscillations in real-time, also known as brain the amygdala shifted connectivity to PFC emotion
waves. Historically, the EEG signal was the first to be regulation areas involved in top-down executive func­
used for neurofeedback in order to regulate neural ac­ tioning. 28 This switch in amygdala connectivity was
tivity and corresponding pathological brain states in positively associated with reduced hyperarousal among
patients with PTSD, 28,32,99–101 culminating in a recent patients and negatively correlated to PTSD symptom
randomized controlled trial in patients with chronic severity. In a wider context, the results were consistent
PTSD.102 with neurocognitive models of PTSD emotion under-
Peniston and Kulkosky100 reported one of the first modulation, which suggest that PTSD symptoms man­
studies that demonstrated significant reductions in ifest from weakened top-down cortical regulation of the
PTSD symptoms following the regulation of alpha subcortically hyperactive amygdala and limbic system.22
brain waves using EEG neurofeedback in Veterans with Critically, this study represents a therapeutic “tuning”
PTSD. After training to increase “slow” brain waves of neural dynamics toward increased top-down regula­
(i.e., alpha and theta waves), only 20% of PTSD patients tion over the limbic (amygdala) and midbrain (periaq­
had a recurrence of PTSD symptoms over a 30-month ueductal grey) systems with associated acute symptom
period, consisting of monthly follow-up assessments, in alleviation.28,105
contrast to 100% of the control group.100 Furthermore, In accordance with this model, EEG neurofeed­
the neurofeedback group also displayed more significant back training of amygdala-correlated activity leads to
improvements on the Minnesota Multiphasic Personal­ emotion regulation improvements in soldiers during
ity Inventory (MMPI) scales, as compared to controls.99 combat training.26 Taken together, EEG neurofeedback
More recently, a mechanistic study on alpha-based neu­ represents a non-invasive way to normalize dysregulat­
rofeedback in PTSD patients was found to rescue alpha ed activation in emotion regulation areas of the PFC, as
oscillations post-training, which was directly associated well as in limbic and midbrain brain structures involved
with significant reductions in hyperarousal symptoms.32 in innate fear and reflexive responding to trauma (amyg­
Interestingly, this neurofeedback protocol also lead to dala and brainstem periaqueductal grey), with the aim

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Nicholson et al

to correct neural patterns of emotion undermodulation connectivity; and (3) increased PFC activation and
in PTSD.28 functional connectivity to key limbic structures indic­
In support of this, a recent randomized control tri­ ative of increased top-down control of emotion gener­
al on alpha-based EEG neurofeedback in patients with ation regions (Figure 1). In addition, neurofeedback
chronic PTSD showed that, as compared to the control appears to shift amygdala functional connectivity away
group, neurofeedback treatment produced significant from fear-processing and defence regions and towards
improvements for both PTSD symptoms and capacity emotion regulation regions, an effect which is negative­
for emotion regulation.102 Neurofeedback led to sig­ ly correlated to PTSD symptoms and alpha rhythm,
nificant reductions in the number of patients meeting and is associated with increased calmness among PTSD
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

criteria for PTSD — from 88.9% to 27.3% in the exper­ patients. 28,32,71,72
imental neurofeedback group — that was sustained in a Relevant for the implementation of neurofeed­
one-month post-treatment follow-up.102 Participants in back locally in the clinic and remotely among deployed
this study consisted of a number of traumatized indi­ military members, EEG neurofeedback is a relatively
viduals with PTSD who had not responded to at least inexpensive and mobile tool for administering neu­
six months of trauma-focused psychotherapy.102 Only rofeedback. Furthermore, EEG-based neurofeedback
a very small amount (4%) of participants in the active treatment settings are arguably more comfortable envi­
treatment condition reported side effects of increased ronments than the fMRI scanner. Nonetheless, fMRI
flashbacks,102 although additional research is needed to studies are also important for investigating anatom­
elucidate further potential side effects of neurofeedback ically localized neural mechanisms underlying neu­
in trauma samples. Another study demonstrated that 30 rofeedback. Hence, a convergence of EEG and fMRI
sessions of alpha-based EEG neurofeedback lead to in­ neurofeedback modalities are critical for the clinical
creased cognitive functioning and decreased symptoms integration of neurofeedback for PTSD treatment. In­
of depression among PTSD patients.101 Notably, where­ deed, scientists in the field of neurofeedback have begun
as most evidence-based therapies for PTSD focus on to use simultaneous EEG/fMRI recordings to define
the processing of trauma memories, the target of neuro­ patterns of electrical recording that correlate to highly
feedback is neural regulation, stabilization, and homeo­ specific subcortical targets normally only measurable
stasis. Since cognitive self-regulation disruptions have with fMRI.26,27 Importantly, when targeting the amyg­
been identified as an obstacle for psychotherapy-based dala via EEG neurofeedback, results suggest modulation
treatments, neurofeedback may be especially beneficial of neural pathways comodulated during amygdala-based
for PTSD patients who are highly anxious, dissociated targeted rt-fMRI-nfb.26,27 Furthermore, correlations be­
or dysregulated, and who may not tolerate or respond tween amygdala fMRI activity and frontal EEG asym­
to other forms of treatments.22,102,106 Taken together, metry during amygdala-based rt-fMRI-nfb training in
empirical evidence for both EEG and fMRI neurofeed­ patients with depression also suggests that EEG and
back modalities suggest that modern neurofeedback fMRI-based neurofeedback methods have overlapping
technology may facilitate a more personalized medicine mechanisms of modulation.81 Specifically, the study by
approach when treating patients with PTSD and may Zotev et al.81 suggests that EEG-based neurofeedback
utilize similar neural mechanisms/pathways to achieve on frontal EEG asymmetry in the alpha band may be
these therapeutic results. compatible with amygdala-based targeted rt-fMRI-nfb.
It has also been suggested that a combination of the two
CONVERGING EVIDENCE FOR REAL-TIME methods could enhance emotion regulation training in
fMRI AND EEG NEUROFEEDBACK IN THE patients with other psychiatric disorders.81
TREATMENT OF PTSD In terms of future directions, multiple researchers
Interestingly, both f MRI and EEG modalities in Ruth Lanius’ laboratory are analyzing a 20-session
demonstrate very similar neurobiological mechanisms randomized controlled trial of alpha-based EEG neu­
in terms of normalizing disrupted brain circuitry in rofeedback in patients with PTSD to compare against
PTSD. Both amygdala-targeted rt-fMRI-nfb71,72 and sham neurofeedback and healthy controls. fMRI data
alpha-based EEG neurofeedback 28,32 lead to (1) plas­ collected throughout the clinical trial will also be an­
tic modulation of ICNs associated with PTSD symp­ alyzed to elucidate further specific neural mechanisms
tom presentation; (2) functional changes in amygdala related to changes in symptomatology. In this study,

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Regulating PTSD symptoms with neurofeedback
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Figure 1. Converging evidence for neurobiological mechanisms underlying both EEG and real-time fMRI neurofeedback
Solid red lines indicate increased functional connectivity, while broken red lines indicate decreased connectivity between
brain regions. Alpha-based EEG neurofeedback that targets abnormal cortical oscillations leads to a shift in amygdala
connectivity toward emotion regulation areas and away from threat, fear, and defence processing regions, as well as areas
implicated in trauma memory. Decreased DMN activity during EEG neurofeedback is associated with a homeostatic
normalization of such activity, with increased SN connectivity and decreased hyperarousal in PTSD patients. Amygdala-
based real-time fMRI neurofeedback that targets a localized brain region highly implicated in PTSD emotional responses,
which similarly involves increased amygdala connectivity to, and activation within, emotion regulation areas. Furthermore,
downregulating the amygdala in PTSD patients is associated with increased CEN and SN recruitment as well as normalized
DMN recruitment. In sum, both modalities of neurofeedback lead to a reorganization of amygdala functional connections, in
addition to increased emotion regulation activity and plastic modulation of ICNs.
EEG = electroencephalography; DMN = default mode network; SN = salience network; CEN = central executive network;
ICN = intrinsic connectivity network; PTSD = posttraumatic stress disorder.

it will also be critical to examine PTSD heterogeneity, associated reductions in symptoms. As such, there is an
and unique responses to treatment among PTSD and its urgent need for further investigation of neurofeedback
dissociative subtype.1,19–22 in order to fully validate and define the neural mecha-
In summary, observations of altered patterns of nisms underlying the therapeutic effect for PTSD. The
neural functioning within PTSD patients have driven result of such scientific efforts could lead to a frontline,
efforts to develop novel treatment interventions that non-invasive and modern method for treating PTSD
target both abnormal brain oscillations and localized and related psychiatric disorders, for military personnel
anatomical brain regions. Both fMRI and EEG neuro- and Veterans.
feedback modalities display common evidence for un­
derlying neurobiological mechanisms, where both have REFERENCES
been shown to lead to plastic changes in ICNs, as well 1. American Psychiatric Association. Diagnostic and
as changes in emotion regulation regions and amygda- statistical manual of mental disorders. 5th ed. Wash-
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photon emission computed tomography in posttrau­
matic stress disorder before and after treatment with a Andrew A. Nicholson, PhD, completed his studies in
selective serotonin reuptake inhibitor. J Affect Disord. neuroscience at the Schulich School of Medicine and
2004;80(1):45–53. https://doi.org/10.1016/s0165­ Dentistry at the University of Western Ontario. His research
0327(03)00047-8. Medline:15094257 background includes a multitude of brain imaging studies in
97. Daniels JK , Mcfarlane AC, Bluhm RL, et al. Switching the field of psychiatric medicine, with expertise in a range of
between executive and default mode networks in post­ technical brain imaging methods, including real-time fMRI
traumatic stress disorder: alterations in functional con­ neurofeedback, dynamic causal modelling, and machine
nectivity. J Psychiatry Neurosci. 2010;35(4):258–66. learning.
https://doi.org/10.1503/jpn.090010. Med­ Tomas Ros, PhD, is a neuroscientist investigating EEG-
line:20569651 based neurofeedback for the treatment of psychiatric

14 Journal of Military, Veteran and Family Health


doi:10.3138/jmvfh.2019-0032 6(Suppl 1) 2020
Regulating PTSD symptoms with neurofeedback

disorders such as PTSD and ADHD. He is currently based the treatment and research of posttraumatic stress disorder
at the University of Geneva, Switzerland. (PTSD) and related comorbid disorders. She currently holds
Rakesh Jetly, MD, FRCPC, is Senior Psychiatrist and Mental the Harris-Woodman Chair in Mind-Body Medicine at the
Health Advisor, Canadian Armed Forces, Ottawa. He is an Schulich School of Medicine & Dentistry at the University
Associate Professor of Psychiatry at Dalhousie University and of Western Ontario.
at the University of Ottawa. He is also the Chair for Military
Mental Health with the Royal’s Institute of Mental Health COMPETING INTERESTS
Research in Ottawa. He is committed to evolving mental None declared.
health research by investigating the biological underpinnings
This article has been peer reviewed.
of mental health disease, by incorporating technology to
https://jmvfh.utpjournals.press/doi/pdf/10.3138/jmvfh.2019-0032 - Saturday, March 21, 2020 4:20:46 PM - IP Address:213.182.207.12

modernize treatment and diagnostic modalities, and by


CONTRIBUTORS
finding strategies to advance precision medicine.
All authors contributed to the manuscript and approved the
Ruth A. Lanius, MD, PhD, is the director of the post­
final version submitted for publication.
traumatic stress disorder (PTSD) research unit at the
University of Western Ontario. She established the
Traumatic Stress Service and the Traumatic Stress Service FUNDING
Workplace Program, which are services that specialize in None declared.

Journal of Military, Veteran and Family Health 15


6(Suppl 1) 2020 doi:10.3138/jmvfh.2019-0032

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